2850 Pathophysiology Exam Two Flashcards
(190 cards)
1
Q
Tension headache pathophysiology
A
Stress induced, and often associated with muscle tension in neck, shoulders, and occipital area
2
Q
Tension headache: clinical manifestations
A
Bifrontal or occipitofrontal pain with gradual onset
Pressure or band like pain
Vital signs and neuro exam normal
3
Q
Tension headache: risk factor
A
Stress
4
Q
Cluster headache: pathophysiology
A
Pathophysiology not entirely understood, but believed to be a neurovascular disorder
5
Q
Cluster headaches: clinical manifestations
A
Severe, unilateral pain that is usually periorbital and radiates into the jaw, face, etc Eye tearing Eye redness Runny nose Pupil constriction Restlessness Eyelid edema
6
Q
Cluster headache: risk factors
A
Alcohol Tobacco Stress Allergies Weather changes
7
Q
Migraine headaches: pathophysiology
A
Pathophysiology not totally understood, but could be due to low serotonin levels in the brain leading to constriction and dilation of blood vessels
8
Q
Migraine headache: clinical manifestations
A
Unilateral, vascular, throbbing pain that lasts for 4-72 hours May be preceded by aura Nausea and vomiting Light sensitivity Noise sensitivity
9
Q
Migraine headache: risk factors
A
Low serotonin in brain Stress Hormones Smoking Weather Food additives Alcohol Caffeine Fatigue
10
Q
Lupus: pathophysiology
A
Formation of autoantibodies that form immune complexes that are deposited in organs and tissues, which triggers an inflammation response that damages organ membranes and microvasculature
11
Q
Which organs and tissues are most commonly affected by lupus?
A
Skin
Synovium
Glomeruli
Lungs
12
Q
Lupus: clinical manifestations
A
Fatigue Fever Myalgias Arthralgias Butterfly rash Joint inflammation Musculoskeletal pain Splenic enlargement Pleurisy and pleural effusion Vasculitis Pericarditis Anemia Thrombocytopenia Headaches Leukopenia Nephrotic syndrome Raynaud’s phenomenon
13
Q
Nephrotic syndrome
A
Hypertension plus hematuria
14
Q
Ranaud’s phenomenon
A
Tricolor change in the fingers due to vasospasm of blood vessels
15
Q
Lupus: risk factors
A
Genetic predisposition EBV antibodies Being a woman of childbearing age African American, Asian, or Hispanic descent Estrogen Certain prescription medications Environmental elements
16
Q
Fibromyalgia: pathophysiology
A
Unknown
17
Q
Fibromyalgia: clinical manifestations
A
Long-term, body wide pain affecting joints, muscles, tendons, and soft tissues
Fatigue
Headache
Sleep problems
Depression
Anxiety
Pain at at least 11 out of 18 specific tender points
18
Q
Fibromyalgia: risk factors
A
Can affect anyone, but especially women between 20 and 50 years of age
19
Q
What is the most important function of hemoglobin?
A
Combining with oxygen in the lungs and releasing it to peripheral tissues
20
Q
What happens with PaO2 drops below 60 mmHg?
A
Hemoglobin drops off oxygen molecules too quickly, leading to tissue hypoxia
21
Q
What is the role of erythropoietin in the stimulation of RBC production?
A
When bloodstream oxygen gets too low, the kidneys secrete erythropoietin, which stimulates the bone marrow to make red blood cells, increasing the oxygen carrying capacity of blood
22
Q
What is the ventilation-perfusion ratio (V-Q ratio)?
A
Ratio of amount of air reaching the alveoli to the amount of blood reaching the alveoli
23
Q
What is ideal in terms of the VQ ratio?
A
Equal amounts of air and blood reaching alveoli
24
Q
What is the built in compensatory mechanism of the lungs to try to match blood flow and ventilation?
A
When there is little ventilation, pulmonary arterial vessels constrict, redistributing blood flow to better ventilated areas
25
What is the primary stimulus to control rate and depth of breathing?
Central chemoreceptors
26
How do central chemoreceptors work?
They sense changes in CO2 levels and blood pH and adjust rate and depth of breathing
27
Give an example of how breathing will be adjusted based on CO2 and pH
If CO2 levels are high/pH is low, respiration rate and depth will increase
28
Hypercapnia
High levels of CO2
29
What is the role of hypercapnia in breathing?
Stimulate breathing process
30
What is the secondary stimulus of breathing?
Peripheral chemoreceptors
31
How do peripheral chemoreceptors work as a stimulus to breathing?
Receptors in the aortic arch and carotid artery respond to decreased arterial oxygen and stimulate respiration
32
Breathing stimulated by peripheral chemoreceptors is known as..
Hypoxic drive
33
What happens when central chemoreceptors are exposed to high levels of CO2 for long periods of time?
They become less responsive, and peripheral chemoreceptors take over as stimulus for respirations
34
At what level of SaO2 do peripheral chemoreceptors take over?
60 mmHg
35
Describe how mycobacterium tuberculosis is passed to other individuals
Inhalation of airborne droplets containing M. Tuberculosis bacilli, which settle in the bronchial tree and proliferate
36
What is the role of white blood cells in responding to infection with M. Tuberculi?
WBC’s wall off the infected area, forming a lesion called a tubercule (WBCs + bacilli+ fibrotic tissue) which scar tissue forms around, making the bacilli inactive
37
What happens when M. Tuberculi bacteria continue to multiply?
They break through the scar tissue tubercule and continue to proliferate and spread, becoming active again
38
What adverse effect happens in tuberculosis infection when macrophages degrade the bacteria?
Enzymes for killing the bacteria also damage the lung tissue, making lung tissue necrotic, and bacteria reinfect the bronchial tree (patient is contagious again)
39
What are presenting signs and symptoms of pulmonary TB?
```
Chronic cough with purulent sputum
Hemoptysis
Weight loss
Anorexia
Chest pain
Fever with night sweats
```
40
What are some additional findings in patients with pulmonary TB?
Lung crackles
| Enlarged lymph nodes
41
What populations are at high risk for acquiring TB?
```
Healthcare workers
Urban residents
Nursing home residents
Prisoners
Immunosuppressed patients
Those born/living/traveling outside US
```
42
What other lifestyle factors increase the risk of acquiring TB?
```
Living in close quarters with other/infected people
Alcoholism
ESRD
Diabetes
Travel to areas where TB is common
```
43
What are the top causes/triggers of asthma?
```
Allergies
Viral respiratory infections
Exercise
Inhaled chemicals
Multiple episodes of asthma
```
44
What happens in the body (pertaining to asthma) when allergens trigger the immune system?
Bronchial constriction
Inflammation
Increase in size and number of goblet cells that secrete mucus
45
What is the role of T lymphocytes in the pathophysiology of asthma?
They assist B cells to turn into plasma cells that produce immunoglobin E, which triggers the release of histamines and leukotrienes
46
What is the role of leukotrienes during an asthma attack?
Responsible for development of bronchoconstriction, bronchial hyperreactivity, edema, and eosinophilia
47
What substance is stimulated during a viral respiratory infection that can trigger an asthma attack?
IgE directed towards viral antigens
48
What do viral and bacterial upper respiratory infections commonly cause in someone with asthma?
Bronchospasm and copious mucous production
49
How can exercise induce an asthma attack?
Provoking loss of heat and water from the tracheobronchial tree
50
What can exaggerate exercise-induced asthma?
Cold weather
51
How can inhaled chemicals induce bronchospasm?
They irritate receptors that stimulate a vagar reflex, which includes dizziness, sweating, nausea, fainting
52
What can multiple episodes of asthma cause in the airways?
Airway remodeling
53
Describe the process of airway remodeling
Proliferation of respiratory epithelium and hypertrophy of respiratory smooth muscle
54
What is the result of epithelial cell injury in patients with asthma?
It exposes airway to triggers for hyperreactivity, which can cause more frequent bronchospasm
55
What are clinical manifestations of asthma?
```
Wheezing
Cough
Dyspnea
Chest tightness
Prolonged exhalation
```
56
What is an early sign of airway obstruction?
Prolonged exhalation
57
What are signs of a severe asthma attack?
Use of accessory muscles
Distant/diminished breath sounds
Diaphoresis
58
List the signs that a patient is going into respiratory failure
Inaudible breath sounds
Repetitive, hacking cough
Cyanosis
59
What is the most common etiology of asthma?
Allergy
60
Which employment settings have the highest risk for exposure to chemical agents that can cause asthma?
```
Farming
Painting
Construction
Landscaping
Janitorial work
```
61
What are common triggers of asthma in children?
Viral infections, like rhinovirus or RSV
62
Define COPD
A combination of chronic bronchitis, emphysema, and hyperactive airway disease. It is a poorly reversible airflow limitation
63
What are characteristic features of COPD?
Mucus hypersecretion
Hypoxia
Cyanosis
Persistent cough
64
What are some characteristics of emphysema?
Overdistended alveoli with trapped air
| Hyperreactivity in the airways
65
What is the consequence of overdistended alveoli with trapped air?
Obstruction of expiratory airflow
Loss of alveolar elastic recoil
High residual volume of CO2
Summary: breathing in is okay but breathing out is hard
66
What happens with hyper reactive airways in emphysema?
Extremely reactive to irritants, leading to episodes of bronchoconstriction
67
What pathological changes lead to airflow limitation in COPD?
Narrowing
Excessive mucus and fibrosis in airways
Loss of alveolar elastic recoil
Smooth muscle hypertrophy
68
How are pulmonary structures remodeled in COPD?
Bronchioles are remodeled due to chronic inflammation, thickened bronchiole walls, and constricted lumen
69
What factors cause the damages to lung structures in COPD?
Leukotrienes
Interleukins
Tumor necrosis
70
What happens when increased levels of CO2 become chronic in COPD?
Respiratory drive stimulus changes from PCO2 accumulation to low levels of PO2 instead. Hypoxia stimulates breathing
71
Why must administration of oxygen to patients with COPD be carefully controlled?
Oxygen can depress patient’s independent drive to breathe, leading to respiratory arrest
72
What are characteristic s/s of COPD?
```
Dyspnea
Cough
Wheezing
Hypoxia
Cyanosis
```
73
What cardiac complication can be brought on by COPD?
Right sided heart failure
74
Why might individuals with COPD develop clubbing of the fingers?
Chronic hypoxia
75
What is a major cause of COPD?
Smoking
76
What are additional risk factors/causes of COPD?
```
Occupational or environmental exposure to chemicals or dust
Secondhand smoke exposure
Genetic predisposition
Connective tissue diseases
IV drug use
```
77
What is cystic fibrosis?
An inherited, autosomal recessive, multisystem disease
78
Describe the disruption of cells that leads to CF
Disruption of exocrine gland function and chloride secretion in epithelial cells of respiratory tract, pancreas, sweat glands, salivary glands, intestines, and reproductive system
79
What is the primary problem in CF?
Thick, viscous mucous secretions in multiple organ systems
80
What is the consequence of mucous secretions in CF for the lungs and bronchioles?
Impaired oxygen/CO2 exchange at alveoli
| Promotion of bacterial growth
81
What are the consequences of CF mucous secretions on the GI tract?
Poor digestion due to increased mucous
82
What are consequences of the CF mucous secretions on the pancreatic ducts?
Obstructed ducts, leading to deficiency of pancreatic enzyme and deficient digestion of protein, carbs, and fats
83
What are respiratory signs and symptoms of CF?
```
Cough
Excessive sputum
Chronic infection
Wheezing
Air trapping
Sinus disease
Pallor
```
84
What are GI signs and symptoms of CF?
```
Failure to thrive
Fat soluble vitamin deficiency
Edema
Pancreatitis
Rectal prolapse
Loose and fatty stools
```
85
Why are women of childbearing age at higher risk for iron deficient anemia?
Menstrual blood loss
| Increased iron needs in pregnancy/delivery/breastfeeding
86
Why are infants and children at risk for iron deficient anemia?
Low iron in cows milk (after weaning from formula or breast milk)
Increased iron need during growth
87
Why are elderly adults at risk for iron deficient anemia?
Poor diet
Dental issues
Lack of stomach acid (which is needed for iron absorption)
88
What are some causes of GI bleeding?
Peptic ulcers
Esophageal varices
GI cancer
89
What is the first thing to do when a man presents with iron deficiency?
Check for GI bleeding
90
What is the RDA of iron intake for men and women?
Men: 8 mg/day
Women: 18 mg/day
91
What are signs and symptoms of anemia in general?
Fatigue
Weakness
Exercise intolerance
92
What are specific signs of iron deficiency?
```
Har loss
Cheilitis
Nail changes
Pica
Cold intolerance
Glossitis (tongue inflammation)
```
93
Normal BP parameters
Less than 120/80
94
Stage one hypertension parameters
140-159/90-99
95
Stage two hypertension parameters
Greater than 160/100
96
Primary hypertension
Also known as essential hypertension, it has no known cause
97
Secondary hypertension
Hypertension that is a side effect of a systemic disorder
98
What percentage of adults with HTN have primary HTN?
90-95%
99
What are risk factors for hypertension?
```
Age
African American heritage
Obesity
Diabetes
Inactivity
Tobacco use
High sodium diet
Low potassium or vitamin D intake
Excess alcohol
Stress
```
100
Why are African Americans at higher risk for hypertension?
High sodium sensitivity
101
What are two major negative effects of HTN on the cardiovascular system?
High damaging forces against the endothelial lining
| High resistance against the left ventricle
102
What are the effects of high aortic pressure?
Excessive workload in the left ventricle, which can lead to left ventricular failure
103
How does HTN predispose systemic arteries to injury?
It creates a high shearing force against artery walls, which causes endothelial weakening and injury, which can specifically cause blindness, kidney failure, stroke, and lower extremity vascular issues
104
What are signs and symptoms of target organ damage in HTN?
```
Chest pain
Dsypnea on exertion
Palpitations
Headache
Vision problems
Dizziness
Weakness
Edema
Leg pain
```
105
What symptoms may people with HTN complain of?
Often none
| In extreme cases: headache, nosebleeds, blurred vision, palpitations
106
What change serves as the precursor to atherosclerosis?
Endothelial injury
107
What are common causes of endothelial injury?
Oxidizing free radicals
Shearing force of high BP
High blood glucose levels
Elevated LDL cholesterol
108
Non-modifiable risk factors for atherosclerosis
Age
Gender (males earlier)
Race (African American)
Family history
109
Modifiable risk factors for atherosclerosis
```
Diet
Activity level
Obesity
Lifestyle
HTN
Diabetes
```
110
What is the age difference between men and women in the risk of developing atherosclerosis?
Men over 45 are at higher risk
| Women over 55 or post-menopausal are at increased risk
111
Why are diabetic patients at higher risk for developing atherosclerosis?
Often have elevated triglyceride and LDL levels
| Often have vascular changes
112
Why does smoking increase atherosclerosis risk?
Smoke contains free radicals that cause endothelial injury
| Smoke decreases HDL levels
113
What lifestyle factors contribute to the development of atherosclerosis?
Tobacco use
Excess alcohol use
Stress
114
What is the bodily process of atherosclerosis development?
Endothelial injury brings WBCs and platelets to injury site
WBCs ingest LDL cholesterol
These cholesterol-laden WBCs become foundation for atherosclerotic plaque
115
What happens over time with atherosclerotic plaques?
It enlarges and becomes calcified and turns into a fibrous platelet cap (atheroma)
The expanding plaque stretches the vessel to its limit, and the vessel becomes stiff and hardened
116
What signs and symptoms may be present when atherosclerosis has caused organ dysfunction?
```
Chest pain
SOB
Palpitations
Leg pain
Dependent edema
```
117
What are signs and symptoms when atherosclerosis causes altered cardiac function?
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Obesity
SOB at rest
Pallor
Cyanosis
Weak pulses in lower extremities
Increased BP
Rapid pulse
S4 murmurs and bruits
Chest pain
Dyspnea upon exertion
```
118
Cardiac output
Amount of blood pumped out of left ventricle each minute
119
What is cardiac output based on
Heart rate times stroke volume
120
What controls the heart rate?
SNS and PNS
121
What influences stroke volume?
Preload
Afterload
Cardiac contractility
122
Preload
Volume of blood in the heart at the end of ventricular diastole
123
What does preload mean in the clinical setting?
Volume of blood that enters the right atrium from the venous system
124
Afterload
Amount of resistance ventricles must overcome to pump blood out of the heart
125
What creates high afterload for the right ventricle?
High pulmonary vascular resistance
126
Cardiac contractility
Myocardium’s ability to stretch and contract in response to the heart filling with blood
127
What conditions enhance contractility in a healthy heart?
Increased preload/SV
128
What happens to contractility when afterload increases?
Contractility decreases, so less blood is ejected from the heart
129
What does RAAS stand for?
Renin-angiotensin-aldosterone system
130
Describe renin and its role in BP
Released from kidneys when renal perfusion decreases, triggering angiotensinogen to be released from the liver, which breaks down into angiotensin I, which triggers formation of angiotensin II when it encounters ACE in the lungs
131
What is the role of angiotensin II?
Arterial vasoconstrictor that raises BP, triggers ventricular remodeling, and stimulates adrenal release of aldosterone
132
Aldosterone and it’s mechanism of action
Acts at the nephron to increase sodium and water reabsorption from distal tubules to the bloodstream
133
What are the net effects of the RAAS?
Elevated BP and BV, which leads to increased workload for left ventricle
134
What problem does the RAAS create in left ventricular failure?
The increased BP and BV further weaken the heart muscles
135
Parasympathetic nervous system effects on the heart
Stimulates cholinergic receptors to slow HR and decrease contraction force
136
Sympathetic nervous system effect on the heart
Stimulates beta 1 adrenergic receptors to increase HR and contraction force
137
What role does the posterior pituitary play in blood pressure and blood volume control?
It releases ADH, which causes water reabsorption at the nephron for increased BV and BP
138
What does left ventricular diastolic dysfunction occur from?
Reduced relaxation or increased stiffness of ventricular muscle
139
What is the common cause for development of left ventricle changes?
Increased afterload caused by HTN
140
What does left ventricular systolic dysfunction occur from?
Reduced forward pumping strength of ventricle muscle, leading to decreased stroke volume and cardiac output
141
What are the two major types of consequence of left ventricle systolic dysfunction?
Backwards effect and forward effect
142
Backward effect of left ventricular dysfunction
Buildup of hydrostatic pressure in the left atrium and pulmonary vasculature, leading to fluid accumulation in pulmonary interstitial/intracellular spaces (pulmonary edema)
143
Forward effect of left ventricle systolic dysfunction
Inadequate ejection of blood into the aorta and decreased perfusion through the arterial circulatory system
144
What does left ventricle systolic dysfunction stimulate?
RAAS, ADH release, and SNS activation
145
What are the effects of angiotensin II on the systemic arterial system?
Widespread vasoconstriction
Increased peripheral arterial resistance
Aldosterone release
146
What are clinical manifestations of LVF?
Orthopnea
Paroxysmal nocturnal dyspnea (sudden SOB in middle of night)
Cerebral symptoms: headache, memory loss, insomnia, anxiety, disorientation
GI signs and symptoms
147
Right ventricular failure is also known as
Cor pulmonale
148
Backwards failure in right ventricular failure
Right ventricle is weak, leading to increased pressure in right atrium, which increases systemic venous pressure, leading to edema in the body
149
What is the result of increased pulmonary arterial blood flow?
Hypoxemia (tissue hypoxia)
150
What are clinical manifestations of right ventricular failure?
Jugular venous distension
Poor GI venous drainage
Peripheral edema
151
What conditions are associated with poor GI venous drainage?
```
Anorexia
Nausea
Early satiety
Postprandial fullness
Indigestion
Impaired absorption
```
152
Stress incontinence: manifestations
Incontinence upon force, such as coughing, sneezing, or laughing
153
Stress incontinence: causes
Poor pelvic support or sphincter weakness due to pregnancy, age, or low estrogen levels
154
Urge incontinence: manifestations
Urgency and frequency of urination
155
Urge incontinence: cause
Overactive detrusor muscle, though the exact mechanism is unclear
156
Overflow incontinence: manifestations
Chronic overdistention and urinary retention
157
Overflow incontinence: most common cause
BPH
158
Neurogenic bladder: manifestation
Chronic bladder overdistention
159
Neurogenic bladder: causes
Spinal cord injury or disorder causing interruption of sensory nerve fibers or afferent nerve pathways between bladder and spinal cord
160
Mixed incontinence
Combination of stress and urge incontinence
161
Functional incontinence: manifestation
Incontinence due to not being able to get to the bathroom in time
162
Functional incontinence: causes
CNS damage, (stroke, dementia, immobility, cognitive impairment)
163
BPH: pathophysiology
Excessive cell growth of the prostate gland
164
BPH: etiology
Testosterone-sensitive cellular proliferation and lack of apoptosis in the prostate
165
BPH: clinical manifestations
```
Frequent urination but voiding only small amounts
Incontinence
Incomplete bladder emptying
Dribbling
Straining to urinate
Weak urine stream
Increased UTI/risk
```
166
By age 60, what percent of men have some degree of BPH?
50%
167
Constipation: causes
```
Lack of fiber or fluid
Lack of physical activity
Ignoring urge to defecate
Drugs (especially opiates)
Diseases that slow GI tract
```
168
Constipation: manifestations
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Hard stools
Pain and discomfort
Increased flatulence
Increased rectal pressure
Hemorrhoids
Abdominal distinction and bloating
```
169
What is the most common GI disorder in the US?
GERD
170
GERD: pathophysiology
Lower esophageal sphincter is weak, allowing acid reflux into the esophagus, causing esophageal ulceration.
This causes metaplasia (esophageal epithelial cells turning into stomach-like columnar epithelium)
Delayed gastric emptying also contributes to discomfort and erosion
171
GERD: signs and symptoms
```
Dysphasia
Heartburn
Epigastric pain
Regurgitation
Respiratory complaints
Bitter taste in mouth
```
172
Who is most affected by GERD?
Infants and those over 40
173
What is Barrett’s esophagus?
Changes in esophageal structure in GERD. Precancerous cellular changes
174
GERD: risk factors
```
Obesity
Pregnancy
Nicotine
Alcohol use
Chocolate
Coffee
Fatty foods
Certain meds
```
175
Peptic ulcer disease: description
Inflammatory erosion of stomach or duodenal lining
176
Peptic ulcer disease: pathophysiology
Hypersection of hydrochloric acid, Ineffective GI mucous production, and poor cellular repair cause erosion of the mucous membranes in the stomach and duodenum. HCl leaks into the stomach wall and blood vessels, causing ulcers
177
What often damages the protective mechanisms of the stomach in PUD?
H. Pylori bacteria (secretes urease, which breaks down urea and neutralizes stomach acid)
178
What are some other causes of peptic ulcers?
Excessive NSAIDs
Alcohol abuse
Excess caffeine
Smoking
179
Why does chronic NSAID use cause peptic ulcers?
NSAIDs counteract prostaglandin E secretion, which stimulates gastric mucous production
180
Peptic ulcer disease: signs and symptoms
```
Epigastric or abdominal pain occurring 2-3 hours after eating
Intense burning and gnawing pain
Pain that wakes patient up at night
Nausea and vomiting
Blood in vomit or stool
```
181
Peptic ulcer disease: complications
Bleeding from the ulcer
Perforation
Scarring of stomach lining
Pyloric stenosis
182
Signs and symptoms of peptic ulcer perforation
Sudden, excruciating pain
Abdominal rigidity
Pallor
Cold sweats
183
Signs of gastric peptic ulcers
Pain relief immediately upon eating food, then pain gets worse after acid secretion starts
184
Signs of duodenal peptic ulcers
Pain that is not relieved by food, or food not relieving it until a while has passed after eating
185
Crohn’s disease: definition
Chronic, uncontrolled immune response of the bowel that leads to bowl destruction and sometimes obstruction
186
Crohn’s disease: pathophysiology
Mucosa of bowels is chronically inflamed with high levels of immunoglobins, T-cells, and macrophages. This causes inflammation and destruction of segments of the bowel
187
What are some characteristic features of the bowel of someone with crohn’s?
Granulomas (large masses of immune cells)
| Cobblestone appearance due to sporadic areas of bowel destruction
188
Crohn’s disease: etiology
Unknown, but may be genetic or environmental
| Higher SES or being female increase risk
189
Peak onset for Crohn’s disease
Between 15 and 30 years old, or between 60 and 80 years old
190
Crohn’s disease: signs and symptoms
```
Diarrhea
Abdominal pain
Remissions and exacerbations
Blood in the stool
Weight loss
Abdominal pain
Anorexia
N/V/D
Increased bowel sounds
Arthritis
Cheilitis
```
